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目的:观察重组人脑利钠肽(rhBNP)对氧化型低密度脂蛋白(ox-LDL)诱导的THP-1源巨噬细胞凋亡的影响,并初步探讨其机制。方法:建立ox-LDL诱导巨噬细胞凋亡的模型。收集干预好的细胞,采用流式细胞仪检测各组细胞凋亡率及线粒体膜电位的变化;应用共聚焦显微镜测定细胞内活性氧(ROS)水平。结果:ox-LDL以浓度依赖方式诱导巨噬细胞凋亡,与control组相比,100μg/ml ox-LDL呈现出最大的凋亡率[(45.62±2.76)%∶(6.81±1.94)%,P<0.05]。rhBNP可以抑制ox-LDL诱导的巨噬细胞凋亡,在10~(-9) mol/L抑制作用最大(18.56±1.79)%,P<0.05。与control组相比,100μg/ml ox-LDL组ROS水平升高,而线粒体膜电位降低[(527.30±36.20)%∶(100.00±0.00)%,(3.01±0.52)%∶(9.67±0.51)%,P<0.05];10~(-9) mol/L rhBNP逆转这些变化[(237.30±30.62)%,(6.55±1.57)%,P<0.05]。结论:rhBNP抑制ox-LDL诱导的THP-1源巨噬细胞凋亡,其机制可能与调节氧化应激及抑制线粒体电位降低相关。
AIM: To observe the effect of recombinant human brain natriuretic peptide (rhBNP) on the apoptosis of THP-1-derived macrophages induced by ox-LDL and to explore its mechanism. Methods: A model of ox-LDL-induced macrophage apoptosis was established. The interventional cells were collected. The apoptosis rate and the mitochondrial membrane potential of each group were detected by flow cytometry. The level of reactive oxygen species (ROS) in the cells was detected by confocal microscopy. Results: Ox-LDL induced macrophage apoptosis in a concentration-dependent manner. Compared with control group, ox-LDL showed the highest apoptosis rate [(45.62 ± 2.76)% vs (6.81 ± 1.94)%, P <0.05]. rhBNP could inhibit the apoptosis of macrophages induced by ox-LDL, the maximal inhibitory effect was at 10 -9 mol / L (18.56 ± 1.79)%, P <0.05. Compared with control group, the level of ROS increased in 100μg / ml ox-LDL group and the mitochondrial membrane potential decreased (527.30 ± 36.20)% (100.00 ± 0.00)%, (3.01 ± 0.52)% (9.67 ± 0.51) %, P <0.05]; 10 ~ (-9) mol / L rhBNP reversed these changes [(237.30 ± 30.62)%, (6.55 ± 1.57)%, P <0.05]. CONCLUSION: rhBNP can inhibit the apoptosis of THP-1-derived macrophages induced by ox-LDL, which may be related to the regulation of oxidative stress and inhibition of mitochondrial potential.